Hippocampal and cerebellar extracellular amino acids during pilocarpine-induced seizures in freely moving rats.
Hippocampal and cerebellar extracellular amino acids during pilocarpine-induced seizures in freely moving rats.
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毛果芸香碱诱导自由活动大鼠癫痫发作期间海马和小脑细胞外氨基酸。
DOI：
10.1016/s0014-2999(96)00830-8
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发表时间：
1997
影响因子：
5
通讯作者：
Y. Michotte
中科院分区：
文献类型：
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作者：
I. Smolders;K. van Belle;G. Ebinger;Y. Michotte
通过微透析探针（10 mM, 2 μl/min）在海马内给药毒蕈碱受体激动剂匹罗卡品，引起自由运动大鼠边缘癫痫发作。在匹罗卡平给药期间和给药后监测海马和小脑细胞外谷氨酸天冬氨酸和γ-氨基丁酸（GABA）水平的变化。研究了全身或局部施用抗惊厥药对癫痫发作和氨基酸浓度变化的影响。经腹腔注射苯巴比妥（15 mg/kg / d） 7天后，海马内注射苯巴比妥10 mM和卡马西平1 mM (2 μl/min) 180 min后，匹洛卡平引起的癫痫发作完全消失。预先给予卡马西平（每天5mg /kg）的大鼠仍出现癫痫发作。海马细胞外氨基酸水平的变化提示谷氨酸、天冬氨酸和GABA与癫痫发作无关，但在匹罗卡品癫痫动物模型中可能在癫痫发作维持和/或扩散中发挥作用。海马边缘癫痫引起的单侧小脑和对侧小脑细胞外氨基酸的增加，可能在“反向”脑裂现象中起作用。
Limbic seizures were provoked in freely moving rats by intrahippocampal administration of the muscarinic receptor agonist pilocarpine via a microdialysis probe (10 mM for 40 min at 2 μl/min). Changes in extracellular hippocampal and cerebellar glutamate aspartate and γ-aminobutyric acid (GABA) levels were monitored during and after pilocarpine administration. Effects of systemic or local administration of anticonvulsants on the seizures and concomitant changes in amino-acid concentrations, were investigated. Pilocarpine-induced seizures were completely abolished after intraperitoneal premedication for 7 days with phenobarbital (15 mg/kg per day) and after intrahippocampal administration of 10 mM phenobarbital and 1 mM carbomazepine (180 min at 2 μl/min). Rats premedicated with carbamazepine (5 mg/kg per day) still developed seizures. The changes in extracellular hippocampal amino-acid levels suggest that glutamate, aspartate and GABA are not involved in seizure onset, but may play a role in seizure maintenance and/or spread in the pilocarpine animal model of epilepsy. The increases in extracellular amino acids in ipsi- and contralateral cerebellum following limbic seizures provoked in the hippocampus, probably play a role in the ‘reversed’ diaschisis phenomenon.
影响因子：
--
作者：
J. Olney;Collins Rc;Sloviter Rs
通讯作者：
J. Olney;Collins Rc;Sloviter Rs